Why does Hair turn Gray ? -GREY HAIR RESEARCH
Why does hair turn gray ? What causes grey hair ?Learn why hair start greying prematurely and find out what you can do about it. For more on possible available Grey hair treatments, please see the page: Grey hair Treatments.
Grey or white hair is not actually a true grey or white pigment. In fact, it is clear due to lack of pigmentation and melanin. The clear hairs appear as grey or white because of the way light reflects from the hairs. Grey hair color typically occurs naturally as people age (see “Effects of aging on hair color”, below). For some people this can happen at a very young age. The same is true for white hair. In some cases, grey hair may be caused by thyroid deficiencies, Waardenburg syndrome or a deficiency of B12.
NEW GREY HAIR RESEARCH:
Here we provide the latest articles from the cutting edge of grey hair science:
Why Hair Turns Gray Is No Longer A Gray Area: Our Hair Bleaches Itself As We Grow Older (Feb. 23, 2009)
— Wash away your gray? Maybe. A team of European scientists have finally solved a mystery that has perplexed humans throughout the ages: why we turn gray. Despite the notion that gray hair is a sign of wisdom, these researchers show that wisdom has nothing to do with it.
Going gray is caused by a massive build up of hydrogen peroxide due to wear and tear of our hair follicles. The peroxide winds up blocking the normal synthesis of melanin, our hair’s natural pigment.”Not only blondes change their hair color with hydrogen peroxide,” said Gerald Weissmann, MD, Editor-in-Chief of The FASEB Journal. “All of our hair cells make a tiny bit of hydrogen peroxide, but as we get older, this little bit becomes a lot. We bleach our hair pigment from within, and our hair turns gray and then white. This research, however, is an important first step to get at the root of the problem, so to speak.”The researchers made this discovery by examining cell cultures of human hair follicles. They found that the build up of hydrogen peroxide was caused by a reduction of an enzyme that breaks up hydrogen peroxide into water and oxygen (catalase). They also discovered that hair follicles could not repair the damage caused by the hydrogen peroxide because of low levels of enzymes that normally serve this function (MSR A and B). Further complicating matters, the high levels of hydrogen peroxide and low levels of MSR A and B, disrupt the formation of an enzyme (tyrosinase) that leads to the production of melanin in hair follicles. Melanin is the pigment responsible for hair color, skin color, and eye color. The researchers speculate that a similar breakdown in the skin could be the root cause of vitiligo.”As any blue-haired lady will attest, sometimes hair dyes don’t quite work as anticipated,” Weissmann added. “This study is a prime example of how basic research in biology can benefit us in ways never imagined.”
Why Hair Turns Gray: Communication Between Hair Follicles and Melanocyte Stem Cells Key to Mystery (June 14, 2011)
— A new study by researchers at NYU Langone Medical Center has shown that, for the first time, Wnt signaling, already known to control many biological processes, between hair follicles and melanocyte stem cells can dictate hair pigmentation.
The study was published in the June 11, 2011 issue of the journal Cell.The research was led by Mayumi Ito, PhD, assistant professor in the Ronald O. Pereleman Department of Dermatology at NYU Langone. “We have known for decades that hair follicle stem cells and pigment-producing melanocycte cells collaborate to produce colored hair, but the underlying reasons were unknown,” said Dr. Ito. “We discovered Wnt signaling is essential for coordinated actions of these two stem cell lineages and critical for hair pigmentation.” The study suggests the manipulation of Wnt signaling may be a novel strategy for targeting pigmentation such as graying hair. The research study also illustrates a model for tissue regeneration.”The human body has many types of stem cells that have the potential to regenerate other organs,” said Dr. Ito. “The methods behind communication between stem cells of hair and color during hair replacement may give us important clues to regenerate complex organs containing many different types of cells.”Using genetic mouse models, researchers were able to examine how Wnt signaling pathways enabled both hair follicle stem cells and melanocyte stem cells to work together to generate hair growth and produce hair color. Research also showed the depletion (or inhibition or abnormal) Wnt signaling in hair follicle stem cells not only inhibits hair re-growth but also prevents melanocytes stem cell activation required for producing hair color. The lack of Wnt activation in melanocyte stem cells leads to depigmented or gray hair.The study raises the possibility that Wnt signaling is a key pathway for the regulation of melanocyte stem cells and shows how melanocyte behavior is associated with hair regeneration. This insight provides further understanding of diseases in which melanocytes are either appropriately lost such as hair graying or undergo uncontrolled cell growth as in melanoma.
Researchers have discovered that the kind of “genotoxic stress” that does damage to DNA depletes the melanocyte stem cells (MSCs) within hair follicles that are responsible for making those pigment-producing cells. Rather than dying off, when the going gets tough, those precious stem cells differentiate, forming fully mature melanocytes themselves. Anything that can limit the stress might stop the graying from happening, the researchers said.”The DNA in cells is under constant attack by exogenously- and endogenously-arising DNA-damaging agents such as mutagenic chemicals, ultraviolet light and ionizing radiation,” said Emi Nishimura of Tokyo Medical and Dental University. “It is estimated that a single cell in mammals can encounter approximately 100,000 DNA damaging events per day.”Consequently, she explained, cells have elaborate ways to repair damaged DNA and prevent the lesions from being passed on to their daughter cells.”Once stem cells are damaged irreversibly, the damaged stem cells need to be eliminated to maintain the quality of the stem cell pools,” Nishimura continued. “We found that excessive genotoxic stress triggers differentiation of melanocyte stem cells.” She says that differentiation might be a more sophisticated way to get rid of those cells than stimulating their death.Nishimura’s group earlier traced the loss of hair color to the gradual dying off of the stem cells that maintain a continuous supply of new melanocytes, giving hair its youthful color. Those specialized stem cells are not only lost, they also turn into fully committed pigment cells and in the wrong place.Now, they show in mice that irreparable DNA damage, as caused by ionizing radiation, is responsible. They further found that the “caretaker gene” known as ATM (for ataxia telangiectasia mutated) serves as a so-called stemness checkpoint, protecting against MSCs differentiation. That’s why people with Ataxia-telangiectasia, an aging syndrome caused by a mutation in the ATM gene, go gray prematurely.The findings lend support to the notion that genome instability is a significant factor underlying aging in general, the researchers said. They also support the “stem cell aging hypothesis,” which proposes that DNA damage to long-lived stem cells can be a major cause for the symptoms that come with age. In addition to the aging-associated stem cell depletion typically seen in melanocyte stem cells, qualitative and quantitative changes to other body stem cells have been reported in blood stem cells, cardiac muscle, and skeletal muscle, the researchers said. Stresses on stem cell pools and genome maintenance failures have also been implicated in the decline of tissue renewal capacity and the accelerated appearance of aging-related characteristics.”In this study, we discovered that hair graying, the most obvious aging phenotype, can be caused by the genomic damage response through stem cell differentiation, which suggests that physiological hair graying can be triggered by the accumulation of unavoidable DNA damage and DNA-damage response associated with aging through MSC differentiation,” they wrote.
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